The impact of an aquatic exercise program on BDNF levels in Parkinson's disease patients: short-and long-term outcomes.

The present study aimed to analyze the short-and long-term effects of an aquatic exercise program on plasma brain-derived neurotrophic factor (BDNF) levels in individuals with Parkinson's disease (PD). The aquatic exercise program lasted one month, and consisted of two sessions per week (1 hour per session). Blood samples were collected at four different timepoints: pre-intervention (T0), immediately after the first session (T1), 48 hours after the first session (T2), and 1 month after the intervention (T3). We found a significant decrease in BDNF levels at T2 vs T1 (p<0.05). However, no changes were observed at the other time-points. Our results demonstrated that the intervention reduced plasma BDNF levels in PD individuals in a time-dependent manner: specifically, we observed acute effects, but no delayed effects.

Does a single bout of exercise impacts BDNF, oxidative stress and epigenetic markers in spinal cord injury patients?

Our aim was to evaluate the impact of a single bout of exercise, consisting of a gait training session with body weight support (BWS), on histone acetylation status (global histone H4 and H3 acetylation levels), brain-derived neurotrophic factor (BDNF) levels, and oxidative stress markers in peripheral blood of individuals with chronic spinal cord injury (SCI). We also set out to compare these responses with those recorded after gait training performed using a walker and with no BWS. The subjects (nearly all with an incomplete spinal cord lesion) were each submitted to two 60-minute experimental sessions on separate days with a 1- week wash-out period between the interventions. The order of the sessions was randomized. Blood samples were collected before and after each experimental trial for measurement of biomarkers. The histone acetylation status and BDNF levels remained unchanged after both interventions. After the treadmill training, the participants showed a strong increase in levels of oxidative stress markers [plasma advanced oxidation protein products (AOPPs), nitrite and thiobarbituric acid-reactive substances] without changes in antioxidant mediators. Instead, elevations in AOPP and nitrite concentrations, in addition to increased levels of glutathione and catalase activity, were found after the walker training. A single bout of gait training, be it conducted on a treadmill with BWS or using a walker without BWS, is not able to alter BDNF levels and histone acetylation status in SCI patients. However, these trials can modulate oxidative stress parameters, seemingly in a protocol-dependent manner.

Treadmill exercise alters histone acetyltransferases and histone deacetylases activities in frontal cortices from wistar rats.

Studies have pointed out the relationship between neuroprotective exercise effects and epigenetic mechanisms on the hippocampus. Considering the role of frontal cortex on brain functions, we investigated the impact of different exercise protocols on enzymatic system involved with histone acetylation status, histone acetyltransferases (HATs), and histone desacetylases (HDACs) in frontal cortices from Wistar rats. Male Wistar rats aged 3 months were submitted to a single session or a daily running protocol during 2 weeks. The single session enhanced HAT activity, while the moderate daily exercise protocol reduced the HDAC activity. Our results indicate that frontal cortex is susceptible to epigenetic modulation following exercise and that both exercise protocols seem to induce a histone hyperacetylation condition in this brain area.

Histone deacetylase activity is altered in brain areas from aged rats.

It has been described that histone acetylation levels are decreased in several cellular and in vivo neurodegeneration models as well as in normal brain aging, although the impact of the aging process on histone deacetylases (HDAC) activity yet remains poorly understood. Therefore, our aim was to evaluate the effect of the aging process on HDAC activity in hippocampi and frontal cortices from 3 and 18-months-old Wistar rats. The animals were decapitated at different times of day, in the early morning and in afternoon. HDAC activity was increased in hippocampus from the aged group. Besides, the hippocampal HDAC activity was also significantly increased in early morning. A significant interaction between age and time of the day was observed in frontal cortices, given that the HDAC activity was higher in early morning in the aged group. These data support the hypothesis that the aging-related dysfunction may be related, at least in part, to acetylation imbalance through HDAC activity in rat brain.